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Archive > Volume 22 Issue 5 > 2015,22(5):584-589. DOI:10.3872/j.issn.1007-385X.2015.05.006 Prev Next
Basic Research
miRNA-101 influence the biological function of lung cancer cells through down-regulate COX-2 expression
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Abstract:
Objective:To investigate the expression of miRNA-101(miR-101) in lung cancer specimens and lung cancer cell lines as well as its impact on the proliferative, colony-forming and tumorigenic capacities of human lung cancer cells. Methods: Cyclooxygenase-2 (COX-2) and miR-101 mRNA and protein levels were assessed, respectively, by RT-PCR and Western blotting in clinical specimens (lung cancer tissue and the surrounding normal tissue) collected from 10 patients, human lung cancer cell lines A549 and NCI-H226, and human diploid MRC-5 fibroblasts. A549 and NCI-H226 cells were transfected with miR-NC and miR-101 respectively. The transfectants were assessed for COX-2 protein content by Western blotting, proliferative activity by CCK-8, colony-forming capacity by colony formation experiments, and tumorigenic capacity in vivo by xenograft experiments in nude BAL B/C mice. Results: COX-2 protein content was significantly higher in cancer tissue specimens than in both para-cancer tissue specimens (t=20.03, P=0.001) and human diploid MRC-5 fibroblasts (t=14.59, P=0.012). In contrast, the expression of miR-101 was down-regulated in lung cancer tissue specimens and cell lines as compared with para-cancer tissue specimens (t=18.33, P=0.002) and human diploid MRC-5 fibroblasts (t=28.95, P=0.000). Overexpression of miR101 resulted in a significant decreases in COX-2 expression (t=26.03, P=0.000) and proliferative (F=5.783, P=0.017) and colony-forming (Dunnett t test I-J=－0.28, P=0.035) capacities of A549 and NCI-H226 lung cancer cells in vitro. A549 cells overexpressing miR101 had a remarkably reduced tumorigenic capacity in nude BALB/c mice in vivo (F=14.8, P=0.003). Conclusion:MicroR-101 is downregulated whereas COX-2 is up-regulated in lung cancer. Over-expression of miR-101 results in significant inhibition of proliferation, colony formation and tumorigenesis of lung cancer cells through down-regulation of COX-2 and thus may offer a potential therapeutic option for lung cancer.
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Project Supported:
Project supportd by the Research Foundation of Education Bureau of Henan Provine （No. 1203068）
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